MITOCHONDRIAL DYSFUNCTION LINKED TO NITRIC OXIDE PATHWAYS IN THE NEUROTOXICITY FROM GLUTAMATE

WALTER MANUCHA

Clínica e Investigación en Arteriosclerosis

Elsevier

Año: 2017 vol. 29 p. 92 - 97

0214-9168

Multiple mechanisms underlying glutamate-induced neurotoxicity have recentlybeen discussed. Likewise, a clear deregulation of the mitochondrial respiratory mechanism has been described in patients with neurodegeneration, oxidative stress, and inflammation. This article highlights nitric oxide, an atypical neurotransmitter synthesized and released on demand by the post-synaptic neurons, and has many important implications for nerve cell survival and differentiation. Consequently, synaptogenesis, synapse elimination, and neurotransmitter release, are nitric oxide-modulated. Interesting, an emergent role of nitric oxide pathways has been discussed as regards neurotoxicity from glutamate-induced apoptosis. These findings suggest that nitric oxide pathways modulation could prevent oxidative damage to neurons through apoptosis inhibition. This review aims to highlight the emergent aspects of nitricoxide-mediated signaling in the brain, and how they can be related to neurotoxicity, as well as the development of neurodegenerative diseases development.